Disease relevance of IL26

• IL-26 is a candidate to contribute to the transformed phenotype of human T cells after infection by herpesvirus saimiri [1].

Psychiatry related information on IL26

• Polymorphisms in the interferon-gamma/interleukin-26 gene region contribute to sex bias in susceptibility to rheumatoid arthritis [2].

High impact information on IL26

• The receptor for IL-26 (AK155), a cytokine of the IL-10 family, has not previously been defined [3].
• Therefore, the ability to respond to IL-26 is restricted by the expression of IL-20R1 [3].
• One of these factors, AK155 or IL-26, was discovered because of its overexpression in human T lymphocytes after growth transformation by the simian rhadinovirus herpesvirus saimiri [4].
• RESULTS: Marker D12S2510, which is located 3 kb 3' from the IL-26 gene, was significantly associated with RA in women (corrected P [P(corr)] = 0.008, 2 degrees of freedom [2 df]) but not in men (P = 0.99, 2 df) [2].
• IL-22 and IL-26 (AK155) expression was exclusively detected in T cells, especially upon type 1 polarization, and in NK cells [5].

Biological context of IL26

• IL-26 (AK155) is a novel cytokine generated by memory cells and is involved in the transformed phenotype of human T cells after infection by herpes virus [6].
• Moreover, the T-lymphokine IL-26 is highly likely to play a role in normal and pathological hematology or immunology [1].
• We began by analysing West African and European haplotype structure and patterns of linkage disequilibrium across a 100 kb genomic region encompassing IFNG and its immediate neighbours IL22 and IL26 [7].
• Novel polymorphisms in the IL-10 related AK155 gene (chromosome 12q15) [8].
• We provide here identification and characterization of two microsatellite polymorphisms at the AK155 locus, i.e. D12S2511 and D12S2510 [8].

Anatomical context of IL26

• Regarding T cells, IL-26 was primarily produced by memory cells, and its expression was independent on costimulation [5].

Other interactions of IL26

• As a lymphokine, AK155 may contribute to the transformed phenotype of human T cells after infection by herpesvirus saimiri [9].

References